Reward remains a central puzzle of neuroscience. Understanding its neural bases is key in developing rationale therapies for a broad spectrum of maladies such as drug addiction, obesity, anorexia nervosa, and depression. Salt appetite is a biological drive triggered by a negative body sodium balance that offers a unique model for investigating the central mechanisms of reward. Sodium appetite fulfills all of the criteria for motivation, as do hunger and thirst, but has some distinct advantages. Its adequate stimulus is simple, the sodium ion, and in the external environment, this stimulus is transduced by a single sensory system, taste. In most mammals, including humans, recognition of sodium is innate. Under normal circumstances, animals show at best a mild preference for weak saline solutions and actively avoid strong ones. When a Na-appetite arises, however, even strong salt becomes highly preferred. The question here is how a modest shift in body sodium balance brings about a dramatic increase in the reward value of this sapid stimulus? Unlike vision, audition, and somethesis, taste has direct neural connections with the limbic forebrain, a large system that is critical to the elaboration of motivation and reward. The overall premise is that gustatory afferent activity from the second central gustatory relay, pontine parabrachial nucleus (PBN), reaches neural reward systems via these limbic connections and, during sodium need, transforms the sensory message elicited by NaCl from aversive to rewarding. We already know that lesions of the PBN prevent the expression of Na-appetite, but that damage to the thalamic and cortical gustatory areas does not. We use the release of dopamine (DA) in the nucleus accumbens as a forebrain index of reward. Sham licking sucrose produces a substantial efflux of accumbens DA even in experienced animals. Under normal circumstances, sham intake of 0.15 M NaCl produces only a small DA spike. During Na-appetite, however, salt intake releases an accumbens DA plume rivaling that of sucrose. Based on these facts, we propose three experimental challenges to the overall premise. Specifically, we will use (1) central lesions, (2) microdialysis, and (3) FOS immunohistochemistry to determine if parabrachial gustatory neural activity distributed via the limbic forebrain is necessary and sufficient for the expression of a Na-appetite, and if these same pathways are responsible for modulating the release of accumbens dopamine during the appetite. The specific limbic areas to be tested include the lateral hypothalamus, the amygdala, and the bed nucleus of the stria terminalis. Pleasure is a product of brain activity. Understanding the neural bases of pleasure or reward is key in developing rational therapies for in broad spectrum of maladies such as drug addiction, obesity, anorexia nervosa, and depression. This project investigates the neural bases of reward using the sense of taste because some gustatory stimuli are inherently rewarding or aversive. The research goal is to determine how taste neural activity reaches brain areas that produce reward and how this sensory information is transformed in the process. [unreadable] [unreadable] [unreadable]